Bibliographic details of the publications referred to by author in this specification are collected at the end of the description.
Reference to any prior art, in this specification is not, and should not be taken as an acknowledgment or any form of suggestion that this prior art is common general knowledge or forms a part of the common general knowledge in Australia or any other country.
The alcohol hangover is characterised by headache, tremulousness, nausea, diarrhoea, and fatigue combined with decreased occupational, cognitive, or visual-spatial skill performance. The symptoms of hangover seem to be caused by dehydration, hormonal alterations, deregulated cytokine pathways, and toxic effects of ethanol and its related bi-products, such as acetaldehyde. Physiological characteristics include increased cardiac work with normal peripheral resistance, diffuse slowing on electroencephalography, and increased levels of antidiuretic hormone.
Alcohol (ethanol) abuse and the resultant hangover are a substantial cost to the community. The recent review (Wiese et al, 2000) suggested that in the United States, related absenteeism and poor job performance cost $148 billion annually (average annual cost per working adult, $2000). Although hangover is associated with alcoholism, most of its cost is incurred by the light-to-moderate drinker. Subjects with hangover may pose substantial risk to themselves and others despite having a normal blood alcohol level. In Australia most motor traffic accidents are alcohol related and therefore represent a substantial problem for policing, legal, insurance and health resources. Interestingly no evidence suggests that alleviation of hangover symptoms leads to increased alcohol consumption (Wiese et al, 2000). Therefore, the development of an effective treatment is warranted, particularly a therapy which improves the cognitive and visual-spatial performance which it turn could reduce absenteeism and improve job performance.
Ethanol is metabolised to acetaldehyde by the enzyme alcohol dehydrogenase and acetaldehyde is metablised to acetate by the enzyme acetaldehyde dehydrogenase. These reactions occur predominantly in the liver but can also occur in other tissues. Ethanol and its related metabolic bi-products have many diverse influences on metabolism which include inhibition of insulin action, alteration of glycolytic enzymes and induction of the formation of oxygen radicals. These basic biochemical reactions result in a significant disturbance of neuronal and endocrine activity such as hypothalamic pituitary adrenal axis activity and catecholamine production.
In the work leading up to the present invention the instant inventor has developed a composition to enhance the metabolism of ethanol and inhibit some of the biochemical changes associated with ethanol and its bi-products, said composition being suitable for use in the prophylaxis and/or treatment of one or more symptoms caused or exacerbated by consumption of a toxic compound such as ethanol.